Bruch Membrane Opening Minimum Rim Width in Neuromyelitis Optica.

Retinal Nerve Fiber Layer Damage as Assessed by Optical Coherence Tomography in Eyes with a Visual Field Defect Detected by Frequency Doubling Technology Perimetry but Not by Standard Automated Perimetry

To measure the thickness of retinal peripapillary nerve fibers throughout the course of neuromyelitis optica (NMO). This study was of a cross-sectional design, examining the thickness of the retinal peripapillary nerve fiber layer by optical coherence tomography, in patients with NMO (n = 15; 30 eyes), patients with multiple sclerosis (MS; n = 15; 30 eyes), and a control group (n = 23; 46 eyes). The thicknesses were acquired according to protocol with the fast RNFL (Retinal Nerve Fiber Layer) procedure. The study of visual function includes for each eye a determination of refraction, measurement of visual acuity, measurement of contrast vision, an analysis of color vision, and a frequency-doubling technology perimetry (FDTP). The main outcome measurements were the thickness of the retinal peripapillary nerve fibers, visual acuity, and scores of contrast vision. The average thickness of retinal peripapillary nerve fibers was respectively in the NMO, MS, and control group: 65.44 +/- 24.19, 83.85 +/- 24.12, and 106.24 +/- 12.46 microm (P = 0.01). The average thickness of retinal peripapillary nerve fibers correlated to visual acuity, the scores of contrast vision, the scores of FDTP, and the number of episodes per patient (r = -0.58, P = 0.03). This is the first study to produce measurements of the thickness of retinal peripapillary nerve fibers during optic neuropathies of NMO. The optic neuropathies of NMO are also accompanied by an acute and chronic axonal loss, as clearly illustrated by the OCT.

Objectives To appraise whether plasma exchange (PLEX) effectively improves visual function for acute optic neuritis (ON) in neuromyelitis optica (NMO) or neuromyelitis optica spectrum disorder (NMOSD). Methods and analysis We searched Medline, Embase, Cochrane Library, ProQuest Central, and Web of Science to identify relevant articles published between 2006 and 2020. Eligible studies were in English and evaluated visual outcomes for people with acute ON in NMO or NMOSD treated with PLEX. They also had adequate pre- and posttreatment data. Excluded were studies with 1 or 2 case reports, or incomplete data. Results Twelve studies were qualitatively synthesized (1 RCT; 1 controlled NRSI; 10 observational studies). Five before-and-after observational studies were used for quantitative synthesis. The PLEX in the 5 studies (3 to 7 cycles over 2 to 3 weeks) was performed as second-line or adjunctive therapy for acute ON in NMO/NMOSD. The qualitative synthesis revealed that visual-acuity recovery occurred between one day and 6 months after the first PLEX cycle completion. Thirty-two of 48 participants in the 5 quantitative-synthesis studies received PLEX. Relative to pre-PLEX values, visual-acuity improvements were nonsignificant at these post-PLEX time points: 1 day (SMD 0.611; 95% CI −0.620 to 1.842); 2 weeks (SMD 0.0214; 95% CI −1.250 to 1.293); 3 months (SMD 1.014; 95% CI −0.954 to 2.982); and 6 months (SMD 0.450; 95% CI −2.643 to 3.543). Conclusions There were inadequate data to determine whether PLEX effectively treats acute ON in NMO/NMOSD.

PurposeCompare the retinal nerve fibre layer (RNFL) thickness in multiple sclerosis (MS) patients, with and without previous episodes of optic neuritis (ON), to disease‐free controls, using optical coherence tomography (OCT).MethodsThe RNFL was measured with a spectral domain OCT (Canon HS‐100) in 433 MS patients and in 70 controls. The MS eyes were sorted into three groups: MS non ON eyes (MSON−), MS ON eyes (MSON+) and the fellow eye of MS ON (MSON_fellow). One eye of each patient in the MSON‐group and in the control group was selected randomly for analysis.ResultsSeventy control eyes, 327 MSON‐ eyes, 106 MSON+ eyes and 106 MSON_fellow eyes were analysed in a linear regression adjusting for age. The average RNFL thickness was found to be statistically thinner in the MSON− group (88.2 ± 13.0 µm) compared to the controls (98.1 ± 9.0 µm; p < 0.00).The average RNFL was thinner in the MSON+ group (77.3 ± 15.2 µm) compared to MSON− eyes and the controls (p < 0.00). A paired t‐test showed a significant decrease in RNFL thickness in the MSON+ eyes compared to MSON_fellow.ConclusionsMultiple sclerosis causes RNFL loss. A mean reduction of ~10 µm was found in MS patients without history of ON and a mean reduction of 20 µm was found in MS patients with history of ON compared to healthy controls. This study showed that OCT is a useful tool that provides evidence of neural degeneration in MS patients, with or without the presence of ON.

Inefficacy of Longitudinal Cup-to-Disc Ratio Measurements in Identifying Glaucoma Progression.

Neuromyelitis optica spectrum disorders (NMOSD) are most often characterized by severe involvement of the optic nerves and/or spinal cord in a mono- or multiphasic manner and associated with anti-aquaporin 4 (AQP4) antibody (Ab) positivity. Optical coherence tomography (OCT) showed moderate to severe retinal axonal loss in neuromyelitis optica spectrum disorders (NMOSD) after optic neuritis (ON) episode. Peripapillary retinal nerve fiber layer (RNFL) and macular thinning seem more marked in NMOSD than in multiple sclerosis (MS) and sometimes (8.7–25.6 %) accompanied by a nonspecific macular change: microcystic macular edema (MME). NMOSD patients without ON might present subclinical retinal axonal loss, but it remains a matter of debate and seems clearly to occur in a lower intensity than in MS. The mechanism of this subclinical involvement remains unclear but could be due to anti-AQP4 antibodies and AQP4 expression on astrocytes inside the optic nerve and RNFL and on retinal Muller cells. OCT may help to differentiate NMOSD from MS by rigorous analysis of eyes with multiple sclerosis associated ON (MSON) and without MSON. In NMOSD, correlations between visual disability and OCT parameters are strong, whereas correlations between clinical disability and OCT parameters remain to be discussed. A few brain magnetic resonance imaging (MRI) studies coupled to OCT investigated optic ways imaging and found interesting correlation between retinal axonal loss and brain white and gray matter parameters. OCT is a wonderful tool enabling us to quantify retinal axonal loss in NMOSD. The main limitations of OCT studies in NMOSD are the small size of NMOSD cohort and sometimes a severe residual visual acuity enabling not to perform OCT.

The anterior optic pathway is one of the preferential sites of involvement in CNS inflammatory demyelinating diseases, such as multiple sclerosis and neuromyelitis optica, with optic neuritis being a common presenting symptom. What is more, optic nerve involvement in these diseases is often subclinical, with optical coherence tomography demonstrating progressive neuroretinal thinning in the absence of optic neuritis. The pathological substrate for these findings is poorly understood and requires investigation. We had access to post-mortem tissue samples of optic nerves, chiasms and tracts from 29 multiple sclerosis (mean age 59.5, range 25-84 years; 73 samples), six neuromyelitis optica spectrum disorders (mean age 56, range 18-84 years; 22 samples), six acute disseminated encephalomyelitis (mean age 25, range 10-39 years; 12 samples) cases and five non-neurological controls (mean age 55.2, range 44-64 years; 16 samples). Formalin-fixed paraffin-embedded samples were immunolabelled for myelin, inflammation (microglial/macrophage, T- and B-cells, complement), acute axonal injury and astrocytes. We assessed the extent and distribution of these markers along the anterior optic pathway for each case in all compartments (i.e. parenchymal, perivascular and meningeal), where relevant. Demyelinated plaques were classified as active based on established criteria. In multiple sclerosis, demyelination was present in 82.8% of cases, of which 75% showed activity. Microglia/macrophage and lymphocyte inflammation were frequently found both in the parenchymal and meningeal compartments in non-demyelinated regions. Acute axonal injury affected 41.4% of cases and correlated with extent of inflammatory activity in each compartment, even in cases that died at advanced age with over 20 years of disease duration. An antero-posterior gradient of anterior optic pathway involvement was observed with optic nerves being most severely affected by inflammation and acute axonal injury compared with the optic tract, where a higher proportion of remyelinated plaques were seen. In neuromyelitis optica spectrum disorder, cases with a history of optic neuritis had extensive demyelination and lost aquaporin-4 reactivity. In contrast, those without prior optic neuritis did not have demyelination but rather diffuse microglial/macrophage, T- and B-lymphocyte inflammation in both parenchymal and meningeal compartments, and acute axonal injury was present in 75% of cases. Acute demyelinating encephalomyelitis featured intense inflammation, and perivenular demyelination in 33% of cases. Our findings suggest that chronic inflammation is frequent and leads to neurodegeneration in multiple sclerosis and neuromyelitis optica, regardless of disease stage. The chronic inflammation and subsequent neurodegeneration occurring along the optic pathway broadens the plaque-centred view of these diseases and partly explains the progressive neuroretinal changes observed in optic coherence tomography studies.

BackgroundMultiple sclerosis (MS) is a common cause of neurological disabilities in adults and commonly affects the visual pathway. The objective of this study is to assess and compare the sensitivity of visual evoked potentials (VEP) and optical coherence tomography (OCT) as measures of early disability in ambulatory patients with MS.MethodsForty-four patients with MS with Expanded Disability Status Scale (EDSS) of ≤ 4.5 (ambulatory patients) and 14 healthy controls participated in this study. Patients were classified into 3 groups according to EDSS. Patients with EDSS of 0–1.5 formed the “No disability,” patients with EDSS of 2–3 formed the “Minimal to mild disability,” and finally patients with EDSS of 3.5–4.5 formed the “Moderate to significant disability” groups. N75/P100 amplitude, P100 latency, retinal nerve fiber layer (RNFL) thickness, and ganglion cell layer complex (GCLC) thickness were measured.ResultsPatients showed significantly lower N75/P100 amplitude, higher P100 latency, lower RNFL, and GCLC thicknesses compared to controls. However, there were non-significant changes in P100 latency, N75/P100 amplitude, and GCLC thickness among the 3 groups for both patients with and without history of optic neuritis (ON). On contrary, RNFL thickness was significantly different between the three groups for both patients with and without history of ON. Factorial ANOVA revealed non-significant disability × History of ON interaction.ConclusionCompared to VEP parameters, RNFL thickness was a sensitive correlate with the various degrees of early disability in fully ambulatory patients with MS whatever the history of ON.

To detect the changes in the retinal nerve fiber layer (RNFL) and ganglion cell complex (GCC) in the eyes of multiple sclerosis patients during the early stage of optic neuritis. A prospective case series study. Suspected acute optic neuritis of multiple sclerosis (MS) patients who attended the department of ophthalmology in Peking Union Medical College hospital from Feb. 2007 to Nov. 2010 were collected. Twenty two MS patients were evaluated within the first week of the attack of acute optic neuritis. The average thickness of RNFL and GCC was measured and a three dimensional image of optic disk was reconstructed using optical coherence tomography (OCT). Within the first week of onset, the average thickness of RNFL and GCC of first attack eyes increased 75% and 64%, respectively. The average thickness of RNFL and GCC in relapsed eyes decreased 91.7% and 62.5% respectively. The average thickness of RNFL and GCC of the fellow eyes also increased 60% and 43% respectively, within the first week of onset. More cases of optic disk edema and thickening of RNFL were found by OCT than by direct ophthalmoscopy. Different changes of the thickness of RNFL and GCC and morphology of the optic disk were detected during the early stage of the initial attack or relapsed optic neuritis in MS patients. OCT could detect such differences.

Structural and Functional Assessment in HIV-Infected Patients Using Optical Coherence Tomography and Frequency-Doubling Technology Perimetry

BackgroundMultiple sclerosis (MS) is an autoimmune disease that attacks the central nervous system, with optic neuritis (ON) being a common early manifestation. Retinal nerve fiber layer (RNFL) thickness may be a biomarker of neuroaxonal damage in MS patients. We sought to evaluate changes in RNFL thickness over 4 years in Omani MS patients with or without ON in comparison to a healthy control group.MethodsThis retrospective case-control study involved 27 MS patients and 25 healthy controls. Optical coherence tomography was performed upon first diagnosis and at a four-year follow-up. Differences in mean RNFL thickness were calculated.ResultsA total of 51 eyes from the MS group and 50 eyes from the control group were evaluated. There was a significant reduction in mean RNFL thickness among MS patients with ON at follow-up (81.21 versus 72.14 μm; P = .003), whereas no significant RNFL thinning was observed among MS patients without ON. However, there was a significant reduction in RNFL thickness among MS patients compared to healthy controls (76.79 versus 93.72 μm; P = .009), regardless of ON presence/absence.ConclusionsAxonal damage was seen in the optic nerves of Omani MS patients. Moreover, there was a significant reduction in RNFL thickness among MS patients with ON as the disease progressed; however, while there was evidence of RNFL thinning in MS patients without ON, this difference lacked statistical significance. Evaluation of RNFL thickness may represent a useful biomarker for monitoring disease progression in MS and its association with ON.

Longitudinal study of retinal nerve fiber layer thickness changes in a multiple sclerosis patients cohort: A long term 5 year follow-up

Glaucomatous Retinal Nerve Fiber Layer Thickness Loss Is Associated With Slower Reaction Times Under a Divided Attention Task

To study the correlation between glaucomatous visual field (VF) defects assessed by standard automated perimetry (SAP) and peripapillary retinal nerve fiber layer (RNFL) thinning measured by spectral domain optical coherence tomography (OCT) using a modified OCT-based peripapillary RNFL structure-function map. Perimetric glaucoma patients and age-matched normal control subjects were recruited from a university hospital clinic. All eyes underwent testing with the Spectralis spectral domain OCT and SAP on the same day. An OCT-based correspondence map, which correlated VF areas with peripapillary RNFL sectors was created to evaluate the relationship between glaucomatous RNFL thinning and VF loss in six nerve fiber layer bundle areas. Correlations of RNFL thinning with corresponding VF defects were examined using Spearman rank-order correlations. To demonstrate the association between localized VF defects and RNFL thickness, the theoretical curves were made according to an established log-linear model. The measured RNFL thickness values and VF defects were presented in the same scatterplot for each sector. Fifty-six glaucoma patients and 85 normal subjects were included in the study. Significant association between localized VF loss and RNFL thinning was found in corresponding areas. Data from the current study fit well with established log-linear models, which compare RNFL thickness values with VF defects. Analysis of RNFL thinning in eyes with localized glaucomatous VF defects showed good structure-function correlation in a new OCT-based structure-function correspondence map.

Although cupping of the optic nerve is classically a sign of glaucomatous optic neuropathy, it has been shown that cupping can sometimes occur after an episode of optic neuritis (ON). The purpose of this study was to compare cupping in patients after ON from multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), or myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and to investigate the relationship between cupping and retinal nerve fiber layer (RNFL) and ganglion cell complex (GCC) thinning. This was a retrospective cohort involving patients (≥18 years) with ON from 3 institutions. Patients were eligible if they had optical coherence tomography (Cirrus, OCT) performed ≥6 months after a single unilateral ON. The amount of thinning and cupping was estimated from the difference in the OCT parameters between affected and unaffected eyes. Univariable and multivariable regressions were used to investigate the relationship between cupping and ON etiology. Pearson correlation was used to investigate the relationship between cupping and RNFL and GCC. Eighty-six subjects (MS: 35, NMOSD: 26, and MOGAD: 25) were included. There was no significant difference in gender and race between the groups, and most patients (86.1%) were female. Patients with NMOSD were significantly older than patients with MS or MOGAD ( P = 0.002). In the univariate model, cupping was significantly higher in the NMOSD group ( P = 0.017); however, after adjusting for age, GCC, and RNFL of the affected eye, the difference was no longer statistically significant ( P = 0.949). The correlation between cupping asymmetry and RNFL and GCC of the affected eye was inversely strong in patients with MS (R = -0.60 and R = -0.64, respectively), inversely moderate in patients with MOGAD (R = -0.34 and R = -0.40, respectively), and weak in patients with NMOSD (R = -0.03 and R = -0.17, respectively). Our results demonstrated that cupping after ON is correlated with RNFL and GCC thinning; although cupping was overall greater in the NMOSD group, once adjusted for age, RNFL, and GCC, it did not differ among patients with MS, NMOSD, and MOGAD.